ArticleInternational journal of ophthalmology2021
Autophagy dysregulation mediates the damage of high glucose to retinal pigment epithelium cells.
Article in International journal of ophthalmology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Dysfunction of the Neurovascular Unit in Diabetic Retinopathy: Advances from Molecular Mechanisms to Targeted Interventions.Stem cell reviews and reports · 2026Review
- Maresin 1 activates autophagy through SIRT1/PPAR-γ signaling to mitigate high glucose-induced pyroptosis in human retinal pigment epithelial cells.Experimental and therapeutic medicine · 2026Article
- Polyphenol-Rich Extract ofNutrients · 2024Article
- The role of autophagy in the treatment of type II diabetes and its complications: a review.Frontiers in endocrinology · 2023Review
- LIN28A attenuates high glucose-induced retinal pigmented epithelium injury through activating SIRT1-dependent autophagy.International journal of ophthalmology · 2023Article
- Article
- The role of the mTOR pathway in diabetic retinopathy.Frontiers in medicine · 2022Review
- Shabyar Ameliorates High Glucose Induced Retinal Pigment Epithelium Injury Through Suppressing Aldose Reductase and AMPK/mTOR/ULK1 Autophagy Pathway.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo observe the role and mechanism of autophagy in retinal pigment epithelial cell (RPE) damaged by high glucose, so as to offer a new idea for the treatment of diabetic retinopathy (DR).
methodsARPE-19, a human RPE cell line cultured
resultsUnder high glucose conditions, the viability of ARPE-19 was decreased, and the apoptosis rate increased, the protein expressions of Bax, Caspase-3, and LC3-II/LC3-I were all increased and the expressions of Bcl-2, p62 and p-mTOR decreased, and autophagic flux was increased compared with that of the controls. Treatment with 3-MA reversed all these changes caused by high glucose.
conclusionThe current study demonstrates the mechanisms of cell damage of ARPE-19 through high glucose/mTOR/autophagy/apoptosis pathway, and new strategies for DR may be developed based on autophagy regulation to manage cell death of RPE cells.
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Registered trials
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